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2.
Journal of Neurology, Neurosurgery and Psychiatry ; 93(9):24, 2022.
Article in English | EMBASE | ID: covidwho-2299498

ABSTRACT

Post-coronavirus disease 19 (COVID-19) syndrome has substantial health and economic implications. It is multi-systemic, with prevalent autonomic symptoms. Understanding presentations and potential autonomic causes may help guide treatment strategies and recovery. All patients with a suspected or confirmed history of COVID-19 infection who underwent autonomic testing between May 2020 and October 2021 were reviewed retrospectively. We evaluated 62 patients (20 male, 42 female, mean age of 41.38 +/-11.52). COVID-19 was PCR confirmed in 15 patients (26%), and five (8%) required acute hospital intervention. Most common symptoms included palpitations (81%), lightheadedness/ dizziness (62%), dyspnoea (48%), fatigue (46%), or cognitive symptoms (33%) Autonomic testing showed normal blood pressure responses to pressor stimuli, a mean respiratory sinus arrhythmia of 18.89b/m, and Valsalva ratio of 2.09. Postural tachycardia syndrome (PoTS) was diagnosed in 12 patients, autonomically mediated syncope (AMS) in 11, neurogenic orthostatic hypotension (NOH) in two, and initial orthostatic hypotension (IOH) in seven. Normal supine and upright plasma noradrenaline levels were measured in 34 patients (mean 283.38 pg/ml supine;472.43pg/ml tilted). Autonomic testing was reassuring (PoTS and syncope) in the majority with abnormal testing (n=32, or 52%). Further phenotyping of PoTS to exclude neuropathic pathology may be needed. IOH and OH are important considerations.

3.
European Respiratory Journal Conference: European Respiratory Society International Congress, ERS ; 60(Supplement 66), 2022.
Article in English | EMBASE | ID: covidwho-2261042

ABSTRACT

Introduction: British Thoracic Society (BTS) guidelines recommend assessment of breathing pattern disorder (BPD) for ongoing breathlessness post COVID-19 infection. 23.7% of patients attending post covid clinic were referred for breathing pattern retraining (BPR) (Heightman et al, 2021) and evidence suggests that BPR can improve breathlessness arising from BPD (British Thoracic Guidance, 2020). Due to large referral numbers and limited specialist work force, virtual group treatment (VGT) was trialled as an alternative to 1:1 intervention. Aim(s): To determine if a VGT improves breathlessness in patients with BPD following COVID-19 infection. Method(s): Data were collected from patients referred for BPR following completion of post Covid-19 multidisciplinary clinic assessment. Breathlessness (Dyspnoea 12- D12) and breathing pattern (Brompton Breathing Pattern Assessment Tool - BPAT) were assessed by a specialist Physiotherapist on referral and on completion of VGT. VGT consisted of 6, 1 hour, physiotherapist led sessions run fortnightly using a virtual platform. The programme included BPR at rest and on exertion, fatigue management and relaxation. Group size was 6-7 participants. A Wilcoxon Sign Rank test was used to compare pre and post treatment data. Result(s): Complete data sets (n=12) were analysed (11 female, 1 male, median age= 52) Improvement in BPAT was statistically significant (median pre 6, post 1, (z=-2.955, p=0.003)). Improvement in D12 was statistically significant (median pre 15, post 7, (z=-2.023, p=0.043)). Conclusion(s): Virtual group BPR treatment improves breathing pattern and breathlessness in the post covid population.

4.
Research and Practice in Thrombosis and Haemostasis Conference ; 6(Supplement 1), 2022.
Article in English | EMBASE | ID: covidwho-2128233

ABSTRACT

Background: Post-COVID syndrome (PCS) is an increasingly recognised complication of acute SARS-CoV- 2 infection, characterised by persistent fatigue, reduced exercise tolerance, chest pain, shortness of breath and cognitive slowing. Acute COVID-19 is strongly linked with increased risk of thrombosis;a prothrombotic state. Elevated Von Willebrand Factor (VWF) Antigen (Ag):ADAMTS13 ratio is associated with severity of acute COVID-19 infection. Aim(s): We hypothesised that the pro-thrombotic state is implicated in the pathogenesis of PCS. We investigated specialist coagulation parameters associated with reduced exercise capacity in patients with PCS to identify the utility of these parameters to determine ongoing disease activity. We also investigated if an association exists between elevated VWF(Ag):ADAMTS13 ratio and impaired exercise capacity in patients with PCS. Method(s): Retrospective analysis of VWF(Ag):ADAMTS13 ratio in patients with PCS at a dedicated post-COVID clinic. VWF(Ag):ADAMTS13 ratio was correlated with symptoms including exercise capacity as assessed by 1 minute sit-to- stand (STS) test and/or 6 minute walk test (6MWT). Peripheral oxygen desaturation >=3% for 6MWT and STS test, and increase in lactate>1 from baseline during 6MWT were taken as markers of impaired exercise capacity. Result(s): Elevated VWF(Ag):ADAMTS13 ratio (>=1.5) was found to be four times (OR 4.3) more likely in patients with impaired exercise capacity. 20% (56/276) had impaired exercise capacity, of which 55% (31/56) had a raised VWF(Ag):ADAMTS13 ratio >=1.5 (p < 0.0001). A higher median VWF(Ag):ADAMTS13 ratio of 1.5 (IQR 1.2-1.7) in patients with abnormal exercise testing compared to 1.1 (IQR 0.9-1.4) in patients with normal exercise testing was found (p < 0.0001). FVIII and VWF(Ag) were elevated in 26% and 18% respectively and support a hypercoagulable state in patients with PCS. Conclusion(s): These findings suggest possible ongoing microvascular/ endothelial dysfunction in the pathogenesis of PCS and highlight the potential role for prophylactic anticoagulation in the management of these patients.

5.
Thorax ; 77(Suppl 1):A202, 2022.
Article in English | ProQuest Central | ID: covidwho-2118472

ABSTRACT

P221 Table 1Virtual group BPR treatment improved breathing pattern and breathlessness for patients within the post covid BPD. With social distancing regulations, VGT offers an effective alternative to face to face group treatment. This saved clinician time which could enable reduced wait times for treatment.British Thoracic Society. British thoracic society guidance on respiratory follow up of patients with a clinico-radiological diagnosis of COVID-19 pneumonia, 2020.Heightman M, Prashar J, Hillman TE, et al. Post-COVID-19 assessment in a specialist clinical service: a 12-month, single-centre, prospective study in 1325 individuals. BMJ Open Resp Res, 2021;8.

6.
Eur Heart J ; 43(Suppl 2), 2022.
Article in English | PubMed Central | ID: covidwho-2107417

ABSTRACT

Background: Long Covid is associated with multiple symptoms and impairment in multiple organs [1]. Cardiac impairment has been reported to varying degrees by varying methodologies in cross-sectional studies. Using cardiovascular magnetic resonance (CMR), we investigated the 12-month trajectory of cardiac impairment in individuals with Long Covid. Purpose: We conducted a prospective, longitudinal, 1-year study in individuals with Long Covid to investigate 1) the characteristics and trajectory of cardiac impairment;2) the impact of acute hospitalisation for COVID-19 on cardiac impairment;and 3) pathways for designing and improving clinical management for individuals at risk of cardiac impairment. Methods: 534 individuals with Long Covid underwent baseline CMR (quantitative T1 and T2 mapping, cardiac mass, volumes, function, and strain) and multi-organ MRI at 6 months (IQR 4.3,7.3) since first post-COVID-19 symptoms. If abnormal findings were reported at baseline, individuals were rescanned at 12.6 months (IQR 11.4, 14.2) (n=330). Symptoms, standardised questionnaires, and blood samples were collected at both timepoints (Figure 1). Cardiac impairment was defined as one or more of: low left or right ventricular ejection fraction (LVEF and RVEF), high left or right ventricular end diastolic volume (LVEDV and RVEDV), impaired left ventricular global longitudinal strain (GLS), or elevated native T1 in ≥3 cardiac independent AHA segments. A significant change over time was reported by comparison with 92 healthy controls. Results: The technical success of this multiorgan assessment in a non-acute setting was 99.1% at baseline, and 98.3% at follow-up, with 99.6% and 98.8% for CMR, respectively. Of individuals with Long Covid, 19% had cardiac impairment at baseline;70% had complete paired data at 12 months. Of those with paired data, 58% presented with ongoing cardiac impairment at 12 months. High sensitivity cardiac troponin I and B-type natriuretic peptide were not predictive of CMR findings, symptoms, or clinical outcomes. At baseline, low LVEF, high RVEDV and reduced GLS were associated with cardiac impairment;however, while elevated T1 was associated with less symptom severity at 12 months, individuals with low LVEF at baseline were associated with ongoing cardiac impairment 1 year post-infection (Figure 2). Conclusion: Cardiac impairment, other than myocarditis, is present in 1 in 5 individuals with Long Covid at 6 months, persisting in over half of those at 12 months. Cardiac-related blood biomarkers are unable to identify cardiac impairment in Long COVID. Subtypes of disease (based on symptoms, examination, and investigations) and predictive biomarkers are yet to be established. Interventional trials with pre-specified subgroup analyses are required to inform therapeutic options. Funding Acknowledgement: Type of funding sources: Public grant(s) – EU funding. Main funding source(s): Radical (EU) and Innovative UK (UK national) (and others)Figure 1Figure 2

7.
Journal of Neurology Neurosurgery and Psychiatry ; 93(9), 2022.
Article in English | Web of Science | ID: covidwho-2005425
8.
EUROPEAN JOURNAL OF NEUROLOGY ; 29:190-190, 2022.
Article in English | Web of Science | ID: covidwho-1965430
9.
American Journal of Respiratory and Critical Care Medicine ; 205(1), 2022.
Article in English | EMBASE | ID: covidwho-1927894

ABSTRACT

Rationale: SARS-CoV-2 infection has been recognised to cause endotheliitis and a pro-thrombotic state during acute illness. Following acute infection, a phenomenon described as 'Long COVID' can cause persisting morbidity with multiple symptoms including exercise intolerance. In recent months preliminary data has proposed persistence of micro-clots as a mechanism for Long COVID. We sought to further understand if a thromboinflammatory processes could be contributing to clinical phenotypes in patients assessed in a UK Post COVID service. Methods: Retrospective analysis of real-world electronic health data relating to patients attending between May 2020 and Jan 2022 (both post hospital and community managed). D-dimer levels, Von Willebrand Factor antigen (vWFAg), date of acute COVID infection and attendance source were available in 1607 patients (1163 community managed and 444 post hospitalisation with acute SARS-CoV-2). vWFAg: ADAMTS13 ratio was reviewed in a subset of 329 patients and correlated with symptoms and functional assessments such as the 6 minute walk test and/or 1 minute sit-tostand test. vWF(Ag):ADAMTS13 ratio was also calculated on 50 voluntary normal controls (Medical Research Ethics Committee Numbers 08/H0810/54 and 08/H0716/72). Results: In the overall cohort D-dimer and vWF(Ag) levels were mostly in the normal range. However, in post-hospitalised patients 21/90 (23.3%) and 65/500(11.5%) community-managed patients had a D-dimer > 550mg/L more than 180 days from acute infection (figure 1). vWF(Ag) levels showed a similar spectrum of abnormalities. In the subgroup with vWF(Ag):ADAMTS13 ratios analysis, 70 (21%) had evidence of abnormal exercise testing as confirmed by desaturation ≥3% and/or an increase in lactate levels >1 above baseline. 43 (61%) of this group had elevated vWF(Ag):ADAMTS13 >1.5. Abnormal exercise testing was associated with a higher vWF(Ag):ADAMTS13 with a median of 1.5 (IQR 1.2-1.7) compared with 1.2 (IQR 0.9-1.4) in those with normal exercise test (p<0.0001), OR 4.955 [2.850-8.612], p<0.0001). Conclusions: This cohort of patients demonstrates a subgroup with persistently elevated D-dimer and vWFAg levels suggesting these markers of thromboinflammatory processes could be of relevance in defining phenotypes within long COVID. The spectrum of abnormality seen, together with the observed correlation of vWF(Ag): ADAMTS13 ratios with impaired exercise tolerance warrants further evaluation of microvascular/ endothelial dysfunction as a mechanism in Long COVID. Further mechanistic studies are in progress.

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